Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent data suggest that the presence of psychotic symptoms in patients suffering from posttraumatic stress disorder (PTSD) may represent an underrecognized and unique subtype of PTSD. Among combat veterans with PTSD, 30% to 40% report auditory or visual hallucinations and/or delusions. The presence of psychotic symptoms in PTSD is associated with a more severe level of psychopathology, similar to that of chronic schizophrenia. In this review, the differential diagnosis of psychotic symptoms in PTSD is discussed, including possible comorbid schizophrenia, psychotic depression, substance-induced psychosis, and personality disorder. A recent biologic study supporting the existence of a unique subtype of PTSD with psychotic features is also addressed, as are the similarities between PTSD with psychotic features and psychotic depression disorder. Finally, data on the treatment implications of psychotic symptoms in PTSD are presented. The intriguing recent findings on psychotic symptoms in PTSD need further investigation in noncombat-related PTSD populations before findings can be generalized to all individuals with PTSD.
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PMID:Psychotic symptoms in posttraumatic stress disorder. 1763 80

Selective serotonin reuptake inhibitors (SSRIs) and antipsychotics co-administration is a widely used strategy to treat both psychotic depression and depressive symptoms in schizophrenia. Nonetheless, the molecular mechanisms involved in the therapeutic benefits of antidepressant-antipsychotic combination are still elusive. It has been suggested that co-administration of SSRIs and antipsychotics may result in molecular changes different from their individual effects. In the present study, we evaluated the acute effects of two SSRIs, citalopram and escitalopram, alone or in combination with haloperidol, on the expression of Homer1a together with its splice variant ania-3, and p11, two genes linked respectively to dopaminergic and serotonergic neurotransmission and involved in synaptic plasticity. Homer1a and ania-3 were induced in the striatum by haloperidol, alone and in combination with SSRIs, but not by SSRIs only. Haloperidol+citalopram co-administration induced a stronger Homer1a expression than haloperidol alone in the ventrolateral caudate-putamen. No signal was detected for p11 in striatum, while there were no significant differences among treatments in cortical subregions. Homer1a was significantly down-regulated in the parietal cortex by all treatments. These results demonstrated that haloperidol+citalopram combination exerts synergistic effects on Homer expression, suggesting that citalopram may influence the impact by haloperidol on the dopaminergic neurotransmission. Moreover, present findings confirm that Homer1a and ania-3 are strongly induced in striatum by haloperidol, while they are not influenced by citalopram or escitalopram in this region. Oppositely, in the cortex the two transcripts are modulated by both haloperidol and SSRIs, suggesting a possible role of both dopamine and serotonin in their cortical regulation.
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PMID:Antipsychotic and antidepressant co-treatment: effects on transcripts of inducible postsynaptic density genes possibly implicated in behavioural disorders. 1918 58

The severity and profile of cognitive dysfunction in first episode schizophrenia and psychotic affective disorders were compared before and after antipsychotic treatment. Parallel recruitment of consecutively admitted study-eligible first-episode psychotic patients (30 schizophrenia, 22 bipolar with psychosis, and 21 psychotic depression) reduced confounds of acute and chronic disease/medication effects as well as differential treatment and course. Patient groups completed a neuropsychological battery and were demographically similar to healthy controls (n=41) studied in parallel. Prior to treatment, schizophrenia patients displayed significant deficits in all cognitive domains. The two psychotic affective groups were also impaired overall, generally performing intermediate between the schizophrenia and healthy comparison groups. No profile differences in neuropsychological deficits were observed across patient groups. Following 6 weeks of treatment, no patient group improved more than practice effects seen in healthy individuals, and level of performance improvement was similar for affective psychosis and schizophrenia groups. Although less severe in psychotic affective disorders, similar profiles of generalized neuropsychological deficits were observed across patient groups. Recovery of cognitive function after clinical stabilization was similar in mood disorders and schizophrenia. To the extent that these findings are generalizable, neuropsychological deficits in psychotic affective disorders, like schizophrenia, may be trait-like deficits with persistent functional implications.
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PMID:A comparison of neuropsychological dysfunction in first-episode psychosis patients with unipolar depression, bipolar disorder, and schizophrenia. 1945 Sep 52

According to earlier observations, minor physical anomalies (MPAs) are more prevalent in psychotic disorders, especially in schizophrenia, and represent an indicator of abnormal fetal development. Limited research has been conducted on these structural abnormalities among patients with unipolar depression, with and without psychotic features. We hypothesized that the mean total MPA score would be greater in patients with psychotic depression than depressive patients without psychosis and control subjects. An extended scale of MPAs was used to detect the presence or absence of 51 MPAs in women with recurrent unipolar depression with psychotic symptoms (n=50), women with recurrent unipolar depression without psychotic symptoms (n=50) and healthy female controls (n=50). Women with recurrent depression had significantly more MPAs than controls. With regard to MPAs of specific body regions, depressive patients had significantly higher rates of MPAs in the mouth area than control subjects. Higher rates of MPAs were not significantly related to psychotic features of depression. The study results are indicative of possible early neurodevelopmental disturbance in recurrent unipolar depression.
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PMID:Minor physical anomalies in women with recurrent unipolar depression. 2007 Oct 35

Delirium represents a symptom of a thought disorder in which a belief is strongly held in spite of invalidating evidence. Many varieties of delirium have been described and this symptom is common in psychotic disorders (schizophrenia, brief psychotic disorder, chronic delusional disorders, etc.), affective disorders (major depressive disorder, psychotic depression, melancholic depression, bipolar disorder, etc.), organic illnesses and psychotropic substance abuse. Delirium has been deeply studied by psychopathology. Our work offers an overview of the most relevant psychopathological descriptions of delirium in the last century, from Jaspers to Kapur.
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PMID:[The psychopathology of delirium. Evolution of the research from Jaspers to Kapur]. 2058 44

Previous studies yielded evidence for dysbindin (DTNBP1) to impact the pathogenesis of schizophrenia on the one hand and affective disorders such as bipolar or major depressive disorder (MDD) on the other. Thus, in the present study we investigated whether DTNBP1 variation was associated with psychotic depression as a severe clinical manifestation of MDD possibly constituting an overlapping phenotype between affective disorders and schizophrenia. A sample of 243 Caucasian inpatients with MDD (SCID-I) was genotyped for 12 SNPs spanning 92% of the DTNBP1 gene region. Differences in DTNBP1 genotype distributions across diagnostic subgroups of psychotic (N = 131) vs. non-psychotic depression were estimated by Pearson Chi(2) test and logistic regression analyses adjusted for age, gender, Beck Depression Inventory (BDI) and the Global Assessment of Functioning Scale (GAF). Overall, patients with psychotic depression presented with higher BDI and lower GAF scores expressing a higher severity of the illness as compared to depressed patients without psychotic features. Four DTNBP1 SNPs, particularly rs1997679 and rs9370822, and the corresponding haplotypes, respectively, were found to be significantly associated with the risk of psychotic depression in an allele-dose fashion. In summary, the present results provide preliminary support for dysbindin (DTNBP1) gene variation, particularly SNPs rs1997679 and rs9370822, to be associated with the clinical phenotype of psychotic depression suggesting a possible neurobiological mechanism for an intermediate trait on the continuum between affective disorders and schizophrenia.
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PMID:Dysbindin (DTNBP1)--a role in psychotic depression? 2095 86

Repetition after attempted suicide is high but only few effect studies have been carried out. The Baerum Model from Norway offers practical and affordable intervention for those not being offered psychiatric treatment. During a period from 2005-2007, all attempted suicide patients except those with major psychiatric diagnoses (schizophrenia, bipolar disorder, severe/psychotic depression), were offered participation. The intervention group received the OPAC programme (outreach, problem solving, adherence, continuity) and the control group received treatment as usual (TAU). The intervention period was 6 months. After this intervention period, all patients were followed passively for an extra 6 months. The design was an intent-to-treat one. The outcomes were: 1) repetition of attempted suicide or suicide, and 2) total number of suicidal acts. A total of 200 patients were offered participation, 67 refused. Of the 133 participants, 69 were randomized to the OPAC programme and 64 to the (non-intervention) control group. Four in each group dropped out after initial participation. There was a significant lower proportion who repeated a suicide attempt the intervention group (proportion 8.7%) than in the control group (proportion 21.9%) and the number of repetitive acts was also significant lower (eight repetitions in the intervention group vs. 22 in the control group). In conclusion, our findings suggest a protective effect of the OPAC programme on the proportion who repeated a suicide attempt and on the total number of repetitions during the follow-up.
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PMID:Preventing repetition of attempted suicide--II. The Amager project, a randomized controlled trial. 2117 37

The following case report describes an act of genital self mutilation. An employed, unmarried male suffering from schizophrenia paranoid type, autocastrated his genitalia during a period of illness when his psychotic symptoms were absent. Sufficient attention may not have been paid to his depressive symptomatology which may be primary as a core feature or secondary, in what can be called post-psychotic depression. The vulnerability of committing such an act increases when the person appears to be symptom-free and regaining insight. After a review of the available literature, it is considered that this case best fits the description for Klingsor Syndrome.
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PMID:A case of Klingsor Syndrome: when there is no longer psychosis. 2157 40

The relationship between depressive symptoms and other symptom categories in schizophrenia have been studied by many authors. According to the existing studies depression in schizophrenic patients is related to the presense of positive symptoms, especifically delusions and hallucinations.As far as negative symptoms concerns it seems that there coexist with the depressive symptoms in any phase of the disease at least in a subgroup of schizophrenic patients. In addition, according to the pyramidal model of Kay, when positive and depressive symptoms coexist, they create theclinical picture of the paranoid subtype of schizophrenia. The same holds for the combination of negative and depressive symptoms, which most frequently describe the residual subtype of the disease. Extrapyramidal symptoms are side effects of antipsychotic drugs (especially the classicalones). According to the existing literature it seems that antipyramidal side effects appear more often in schizophrenic patients with depressive symptoms. The differential diagnosis of depressive symptoms in schizophrenic patients should start with the evaluation of possible presence of organiccauses like somatic disease, medication induced extrapyramidal symptoms, substance abuse. Yet, symptoms of depression need to be differentiated from the negative symptoms of schizophrenia. Psychiatric syndromes like schizoaffective disorder, bipolar disorder and depression with psychotic features need to be also considered. In this case is very important to identify accurately the duration of depressive symptoms as well as the succession of appearance of the depressive vs. psychotic symptoms. Depressive symptoms appear to be bad prognostic sign for the long-term outcome of schizophrenia, because of the increased risk for suicide but also because of the worsening of the quality of life and the general wellbeing of the schizophrenic patient. Depressive symptoms during the acute phase of the disease usually respond to antipsychotic therapy, but in some cases the treating physician may consider the use of atypical antipsychotics. In the case of post psychotic depression the concurrent administration of antidepressants is indicated.
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PMID:[Depression in schizophrenia: Relationship with other symptoms, differential diagnosis, prognosis,treatment]. 2221 20

Cognitive impairment is a core feature of patients with neuropsychiatric diseases such as schizophrenia and psychotic depression. The drugs currently used to treat cognitive impairment have significant limitations, ensuring that the search for more effective therapies remains active. Endoplasmic reticulum protein sigma-1 receptors are unique binding sites in the brain that exert a potent effect on multiple neurotransmitter systems. Accumulating evidence suggests that sigma-1 receptors play a role in both the pathophysiology of neuropsychiatric diseases, and the mechanistic action of some therapeutic drugs, such as the selective serotonin reuptake inhibitors (SSRIs), donepezil and neurosteroids. Among SSRIs, fluvoxamine, a potent sigma-1 receptor agonist, has the highest affinity at sigma-1 receptors. Sigma-1 receptor agonists greatly potentiate nerve-growth factor (NGF)-induced neurite outgrowth in PC12 cells, an effect that is antagonized by treatment with the selective sigma-1 receptor antagonist NE-100. Furthermore, phencyclidine (PCP)-induced cognitive impairment, associated with animal models of schizophrenia is significantly improved by sub-chronic administration of sigma-1 receptor agonists such as fluvoxamine, SA4503 (cutamesine) and donepezil. This effect is antagonized by co-administration of NE-100. A positron emission tomography (PET) study using the specific sigma-1 receptor ligand [11C]SA4503 demonstrates that fluvoxamine and donepezil bind to sigma-1 receptors in the healthy human brain. In clinical studies, some sigma-1 receptor agonists, including fluvoxamine, donepezil and neurosteroids, improve cognitive impairment and clinical symptoms in neuropsychiatric diseases. In this article, we review the recent findings on sigma-1 receptor agonists as potential therapeutic drugs for the treatment of cognitive impairment in schizophrenia and psychotic depression.
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PMID:Sigma-1 receptor agonists as therapeutic drugs for cognitive impairment in neuropsychiatric diseases. 2228 9


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